{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang H"],"funding":["National Natural Science Foundation of China"],"pagination":["1743-1755"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7986127"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["148(7)"],"pubmed_abstract":["Metabolism reprograming is a hallmark of cancer and plays an important role in tumor progression. The aberrant metabolism in renal cell carcinoma (RCC) leads to accumulation of the oncometabolite L-2-hydroxyglurate (L-2HG). L-2HG has been reported to inhibit the activity of some α-ketoglutarate-dependent dioxygenases such as TET enzymes, which mediate epigenetic alteration, including DNA and histone demethylation. However, the detailed functions of L-2HG in renal cell carcinoma have not been investigated thoroughly. In our study, we found that L-2HG was significantly elevated in tumor tissues compared to adjacent tissues. Furthermore, we demonstrated that L-2HG promoted vasculogenic mimicry (VM) in renal cancer cell lines through reducing the expression of PHLDB2. A mechanism study reveale"],"journal":["International journal of cancer"],"pubmed_title":["Oncometabolite L-2-hydroxyglurate directly induces vasculogenic mimicry through PHLDB2 in renal cell carcinoma."],"pmcid":["PMC7986127"],"funding_grant_id":["81702504","81773789","81702508","21402173","81870484","81672520"],"pubmed_authors":["Li G","Xue D","Qian J","Zhang J","Lu Z","Shen D","Zheng Q","Wang H","Jiang M","Ding L","Wang L","Wu H","Xia L","Lu J","Chen Y"],"additional_accession":[]},"is_claimable":false,"name":"Oncometabolite L-2-hydroxyglurate directly induces vasculogenic mimicry through PHLDB2 in renal cell carcinoma.","description":"Metabolism reprograming is a hallmark of cancer and plays an important role in tumor progression. The aberrant metabolism in renal cell carcinoma (RCC) leads to accumulation of the oncometabolite L-2-hydroxyglurate (L-2HG). L-2HG has been reported to inhibit the activity of some α-ketoglutarate-dependent dioxygenases such as TET enzymes, which mediate epigenetic alteration, including DNA and histone demethylation. However, the detailed functions of L-2HG in renal cell carcinoma have not been investigated thoroughly. In our study, we found that L-2HG was significantly elevated in tumor tissues compared to adjacent tissues. Furthermore, we demonstrated that L-2HG promoted vasculogenic mimicry (VM) in renal cancer cell lines through reducing the expression of PHLDB2. A mechanism study reveale","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2026-06-02T16:17:52.528Z","creation":"2025-04-03T21:33:02.802Z"},"accession":"S-EPMC7986127","cross_references":{"pubmed":["33320958"],"doi":["10.1002/ijc.33435"]}}